Study Pinpoints Areas in the Brain Associated With Post-Exertional Malaise

Editor's Comment: All of the Gulf War veterans who participated in this study met the criteria for CFS/ME, therefore the results have profound implications for both illnesses. Based on exercise-induced changes in brain function, researchers identified two subgroups of patients: those with predominant pain, and those with orthostatic intolerance. Patients with predominant pain showed a reduction in gray matter, which is consistent with other chronic pain disorders. Patients with predominant orthostatic intolerance showed cerebellar and brainstem atrophy, which is associated with orthostatic tachycardia and reduction in working memory (cognitive impairment). The authors concluded that exercise stress tests should not only be included in diagnostic evaluation for Gulf War and related illnesses, but that post-exercise brain function tests can serve as a biomarker. "Identifying biomarkers such as these for phenotypic designation is one way to begin untangling the pathophysiological and molecular mechanisms underlying idiopathic disease states such as Gulf War Illness."

You can read the New York Times article, "Researchers Find Biological Evidence of Gulf War Illnesses," HERE.

Exercise Challenge in Gulf War Illness Reveals Two Subgroups with Altered Brain Structure and Function

By Rakib U. Rayhan et al.

Abstract

Nearly 30% of the approximately 700,000 military personnel who served in Operation Desert Storm (1990–1991) have developed Gulf War Illness, a condition that presents with symptoms such as cognitive impairment, autonomic dysfunction, debilitating fatigue and chronic widespread pain that implicate the central nervous system.

A hallmark complaint of subjects with Gulf War Illness is post-exertional malaise; defined as an exacerbation of symptoms following physical and/or mental effort.

To study the causal relationship between exercise, the brain, and changes in symptoms, 28 Gulf War veterans and 10 controls completed an fMRI scan before and after two exercise stress tests to investigate serial changes in pain, autonomic function, and working memory. Exercise induced two clinical Gulf War Illness subgroups.

One subgroup presented with orthostatic tachycardia (n = 10). This phenotype correlated with brainstem atrophy, baseline working memory compensation in the cerebellar vermis, and subsequent loss of compensation after exercise.

The other subgroup developed exercise induced hyperalgesia (n = 18) that was associated with cortical atrophy and baseline working memory compensation in the basal ganglia.

Alterations in cognition, brain structure, and symptoms were absent in controls. Our novel findings may provide an understanding of the relationship between the brain and post-exertional malaise in Gulf War Illness.